Chicken poultry industry produces a vast amount of feather waste and is often disposed into landfills, creating environmental pollution. Therefore, we explored the valorization of chicken feather waste into lipids and keratinous sludge biomass. This study demonstrates the successful utilization of keratinous sludge biomass as a unique precursor for the facile preparation of novel keratinous sludge biomass-derived carbon-based molybdenum oxide (KSC@MoO₃) nanocomposite material using two-step (hydrothermal and co-pyrolysis) processes. The surface morphology and electrochemical properties of as-prepared nanocomposite material were analyzed using HR-SEM, XRD, XPS, and cyclic voltammetric techniques. KSC@MoO₃ nanocomposite exhibited prominent electrocatalytic behavior to simultaneously determine hydroquinone (HQ) and catechol (CC) in environmental waters. The as-prepared electrochemical sensor showed excellent performance towards the detection of HQ and CC with broad concentration ranges between 0.5–176.5 μM (HQ and CC), and the detection limits achieved were 0.063 μM (HQ) and 0.059 μM (CC). Furthermore, the developed modified electrode has exhibited excellent stability and reproducibility and was also applied to analyze HQ and CC in environmental water samples. Results revealed that chicken feather waste valorization could result in sustainable biomass conversion into a high-value nanomaterial to develop a cost-effective electrochemical environmental monitoring sensor and lipids for biofuel.

Many communities around the country are undergoing contentious battles over the installation of artificial turf. Opponents are concerned about exposure to hazardous chemicals leaching from the crumb rubber cushioning fill made of recycled tires, the plastic carpet, and other synthetic components. Numerous studies have shown that chemicals identified in artificial turf, including polycyclic aromatic hydrocarbons (PAHs), phthalates, and per- and polyfluoroalkyl substances (PFAS), are known carcinogens, neurotoxicants, mutagens, and endocrine disruptors. However, few studies have looked directly at health outcomes of exposure to these chemicals in the context of artificial turf. Ecotoxicology studies in invertebrates exposed to crumb rubber have identified risks to organisms whose habitats have been contaminated by artificial turf. Chicken eggs injected with crumb rubber leachate also showed impaired development and endocrine disruption. The only human epidemiology studies conducted related to artificial turf have been highly limited in design, focusing on cancer incidence. In addition, government agencies have begun their own risk assessment studies to aid community decisions. Additional studies in in vitro and in vivo translational models, ecotoxicological systems, and human epidemiology are strongly needed to consider exposure from both field use and runoff, components other than crumb rubber, sensitive windows of development, and additional physiological endpoints. Identification of potential health effects from exposures due to spending time at artificial turf fields and adjacent environments that may be contaminated by runoff will aid in risk assessment and community decision making on the use of artificial turf.

Increased interest in backyard food production has drawn attention to the risks associated with urban trace element contamination, in particular lead (Pb) that was used in abundance in Pb-based paints and gasoline. Here we examine the sources, pathways and risks associated with environmental Pb in urban gardens, domestic chickens and their eggs. A suite of other trace element concentrations (including As, Cd, Cr, Cu, Hg, Mn, Ni, Pb, Zn) are reported from the sampled matrices. Sixty-nine domestic chickens from 55 Sydney urban gardens were sampled along with potential sources (feed, soil, water), blood Pb concentrations and corresponding concentrations in eggs. Age of the sampled chickens and house age was also collected. Commercial eggs (n = 9) from free range farms were analysed for comparative purposes. Study outcomes were modelled using the large Australian VegeSafe garden soil database (>20,000 samples) to predict which areas of inner-city Sydney, Melbourne and Brisbane are likely to have soil Pb concentrations unsuitable for keeping backyard chickens. Soil Pb concentrations was a strong predictor of chicken blood and egg Pb (p=<0.00001). Almost 1 in 2 (n = 31/69) chickens had blood Pb levels >20 μg/dL, the level at which adverse effects may be observed. Older homes were correlated with higher chicken blood Pb (p = 0.00002) and egg Pb (p = 0.005), and younger chickens (<12 months old) had greater Pb concentrations, likely due to increased Pb uptake during early life development. Two key findings arose from the study data: (i) in order to retain chicken blood Pb below 20 μg/dL, soil Pb needs to be < 166 mg/kg; (ii) to retain egg Pb < 100 μg/kg (i.e. a food safety benchmark value), soil Pb needs to be < 117 mg/kg. These concentrations are significantly lower than the soil Pb guideline of 300 mg/kg for residential gardens. This research supports the conclusion that a large number of inner-city homes may not be suitable for keeping chickens and that further work regarding production and consumption of domestic food is warranted.

Metal-responsive transcription factor 1 (MTF1) participates in redox homeostasis and heavy metals detoxification via regulating the expression of metal responsive genes. However, the exact role of MTF1 in Cd-induced cerebral toxicity remains unclear. Herein, we explored the mechanism of Cd-elicited cerebral toxicity through modulating MTF1/MTs pathway in chicken cerebrum exposed to different concentrations of Cd (35 mg, 70 mg, and 140 mg/kg CdCl₂) via diet. Notably, cerebral tissues showed varying degrees of microstructural changes under Cd exposure. Cd exposure significantly up-regulated the expression of metal transporters (DMT1, ZIP8, and ZIP10) with concomitant elevated Cd level, as determined by ICP-MS. Cd significantly altered other cerebral biometals concentrations (particularly, Zn, Fe, Se, Cr, Mo, and Pb) and redox balance, resulting in increased cerebral oxidative stress. More importantly, Cd exposure suppressed MTF1 mRNA and nuclear protein levels and its target metal-responsive genes, notably metallothioneins (MT1 and MT2), and Fe and Cu transporter genes (FPN1, ATOX1, and XIAP). Moreover, Cd disrupted the regulation of expression of selenoproteome (particularly, GPxs and SelW), and cerebral Se level. Overall, our data revealed that molecular mechanisms associated with Cd-induced cerebral damage might include over-expression of DMT1, ZIP8 and ZIP10, and suppression of MTF1 and its main target metal-responsive genes as well as several selenoproteins.

The aims of this study were to determine type and application rate of composted animal manure to optimize sweet potato yield relative to N₂O emissions from upland soils. To this end, the study was conducted on upland soils amended with different types and rates of composted animal manure and located at two geographically different regions of South Korea. Field trials were established at Miryang and Yesan in South Korea during the sweet potato (Ipomoea batatas) growing season over 2 years: 2017 (Year 1) and 2018 (Year 2). Three composted animal manures (chicken, cow, and pig) were applied at the rates of 0, 10, and 20 Mg ha⁻¹ to upland soils in both locations. In both Years and locations, manure type did not affected significantly cumulative N₂O emissions from soil during the sweet potato growing season or the belowground biomass of sweet potato. However, application rate of animal manures affected significantly the cumulative N₂O emission, nitrogen (N) in soil, and belowground biomass of sweet potato. An increase in cumulative N₂O emission with application rates of animal manures was related to total N and inorganic N concentration in soil. The belowground biomass yield of sweet potato but also the cumulative N₂O emission increased with increasing application rate of composted animal manures up to 7.6 and 16.0 Mg ha⁻¹ in Miryang and Yesan, respectively. To reduce N₂O emission from arable soil while increasing crop yield, composted animal manures should be applied at less than application rate that produce the maximum belowground biomass of sweet potato.

Mining activity may cause heavy metal accumulation, which threatens human and animal health by their long-term persistence in the environment. This study aims to assess the impact of polymetallic pollution on chicken (Gallus domesticus) from old lead mining sites in northeast of Tunisia: Jebel Ressas (JR). Samples of soil and chickens were collected from five sites being ranked along a gradient of heavy metal contamination. Heavy metal loads were evaluated in soil samples and in chicken liver and kidney. Biochemical evaluation of oxidative stress parameters termed as Catalase (CAT), Glutathione-S-Transferase (GST), and Malondialdehydes (MDA) accumulation was monitored. Metallothionein protein level was assessed as a specific response to heavy metals. DNA alteration was achieved using MNi frequency in the investigated tissues. Finally, the evaluation of gene expression levels of CAT, GST, mt1, mt4, P53, bcl2, caspase3 and DNA-ligase was performed. Our data showed the highest loads of Cd, Cu, Zn and Pb in tissues of animals from site 3, being more pronounced in kidney. Biochemical data suggested a significant increase in antioxidant enzymes activities in all sites respect to control except in site 3 were CAT and GST were inhibited. DNA alteration was observed in all tissues being very pronounced in animals from site 3. Overall, transcriptomic data showed that genes involved in apoptosis were up-regulated in animals exposed to the most contaminated soils. Our data suggest that chicken and selected biomarkers offer a suitable model for biomonitoring assessment of heavy metals transfer through the food web in mining sites. Finally, the obtained results of heavy metals accumulation and related alterations should be carefully considered in view of the controversial relationship between distribution and toxicology of contaminants in exposed organisms.

Cadmium (Cd), a major environmental contaminant, is closely associated with male reproductive health. Selenium (Se) has been recognized as an effective chemo-protectant against Cd toxicity, but the underlying mechanisms remain unclear. The objective of present study was to illustrate the toxic effect of Cd on testis, and then compare the antagonistic effect among different Se sources on growth performance, testicular damage, ion homeostasis, antioxidative potential, and the expression of selenotranscriptome and biosynthetic related factors in Cd-treated chicken. Male chickens were fed with (Ⅰ) Control group: basal diet; (Ⅱ) Cd group: basal diet with 140 mg/kg CdCl₂; (Ⅲ) YSe + Cd group: basal diet with 140 mg/kg CdCl₂ and 3 mg/kg Yeast-Se; (Ⅳ) NSe + Cd group: basal diet with 140 mg/kg CdCl₂ and 1 mg/kg Nano-Se; (Ⅴ) SSe + Cd group: basal diet with 140 mg/kg CdCl₂ and 3 mg/kg Na₂SeO₃. It was observed that different Se treatments dramatically alleviated Cd-induced testicular developmental disorder, ion homeostasis disorder, hormone secretion disorder and oxidative stress. Simultaneously, Se mitigated Cd-induced testicular toxicity by regulating selenoprotein biosynthetic related factors to promote selenoprotein transcription. Finally, this study indicated that dietary supplementation of Yeast-Se produced an acceptable Se form to protect testis from Cd exposure.

Persistent organic pollutants (POPs) including PCDD/Fs, PCBs and organochlorine pesticides (OCPs) are among the most important and hazardous pollutants of soil. Food producing animals such as chicken, beef, sheep and goats can take up soil while grazing or living outdoors (free-range) and this can result in contamination.In recent decades, large quantities of brominated flame retardants such as polybrominated diphenyl ethers (PBDEs), short-chain chlorinated paraffins (SCCPs) and per- and polyfluorinated alkylated substances (PFAS) have been produced and released into the environment and this has resulted in widespread contamination of soils and other environmental matrices. These POPs also bioaccumulate and can contaminate food of animal origin resulting in indirect exposure of humans.Recent assessments of chicken and beef have shown that surprisingly low concentrations of PCBs and PCDD/Fs in soil can result in exceedances of regulatory limits in food. Soil contamination limits have been established in a number of countries for PCDD/Fs but it has been shown that the contamination levels which result in regulatory limits in food (the maximum levels in the European Union) being exceeded, are below all the existing soil regulatory limits. ‘Safe’ soil levels are exceeded in many areas around emission sources of PCDD/Fs and PCBs. On the other hand, PCDD/F and dioxin-like PCB levels in soil in rural areas, without a contamination source, are normally safe for food producing animals housed outdoors resulting in healthy food (e.g. meat, eggs, milk).For the majority of POPs (e.g. PBDEs, PFOS, PFOA, SCCP) no regulatory limits in soils exist.There is, therefore, an urgent need to develop appropriate and protective soil standards minimising human exposure from food producing animals housed outdoors. Furthermore, there is an urgent need to eliminate POPs pollution sources for soils and to control, secure and remediate contaminated sites and reservoirs, in order to reduce exposure and guarantee food safety.

Di-(2-ethylhexyl) phthalate (DEHP) is a prevalent environmental contaminant that severely impacts the health of human and animals. Taxifolin (TAX), a plant flavonoid isolated from yew, exerts protective effects on cardiac diseases. Nevertheless, whether DEHP could induce cardiomyocyte hypertrophy and its mechanism remains unclear. This study aimed to highlight the specific molecular mechanisms of DEHP-induced cardiomyocyte hypertrophy and the protective potential of TAX against it. Chicken primary cardiomyocytes were treated with DEHP (500 μM) and/or TAX (0.5 μM) for 24 h. The levels of glucose and adenosine triphosphate (ATP) were detected, and cardiac hypertrophy-related genes were validated by real-time quantitative PCR (qRT-PCR) and Western blot (WB) in vitro. The results showed that DEHP-induced cardiac hypertrophy was ameliorated by TAX, as indicated by the increased cardiomyocyte area and expression of atrial natriuretic peptide (ANP), natriuretic peptides A-like (BNP) and β-myosin heavy cardiac muscle (β-MHC). Furthermore, DEHP induced cardiac hypertrophy via the interleukin 6 (IL-6)/Janus kinase (JAK)/signal transducer and activator of transcription 3 (STAT3) pathway in vitro. In addition, DEHP disrupted mitochondrial function and glycometabolism by activating the insulin-like growth factor 1 (IGF1)/phosphatidylinositol 3-kinase (PI3K) pathway and the peroxisome proliferator activated receptors (PPARs)/PPARG coactivator 1 alpha (PGC-1α) pathway to induce cardiac hypertrophy in vitro. Intriguingly, those DEHP-induced changes were obviously alleviated by TAX treatment. Taken together, cardiac hypertrophy was induced by DEHP via activating the IL-6/JAK/STAT3 signaling pathway, triggering glycometabolism disorder and mitochondrial dysfunction in vitro, can be ameliorated by TAX. Our findings may provide a feasible molecular mechanism for the treatment of cardiomyocyte hypertrophy induced by DEHP.

Because most chickens are reared in intensive farms, where a range of feed additives are used routinely, concerns have been raised on the potential public health risk of chicken product consumption. This study was conducted to characterize the contents of trace metals in fresh chicken tissues (354 samples) on the food markets in Guangdong province of southern China, a major region of chicken production with heavy per capita chicken consumption, and to assess the public health risk from chronic dietary exposure to the trace metals through chicken consumption. With the exception of Cr, Ni, and Pb, the contents of trace metals were generally higher in the chicken giblets (livers, gizzards, hearts, and kidneys) compared to muscles (breasts and drumsticks). Chicken tissues from the urban markets generally contained higher levels of As, Cu, Mn, and Zn than those from the rural markets, while the contents of Pb were typically higher in the chicken muscles from the rural markets. Results of statistical analyses indicate that Cu, Zn, and As in the chicken tissues derived mainly from the feeds, which is consistent with the widespread use of Cu, Zn, and phenylarsenic compounds as feed supplements/additives in intensive poultry farming. No non-carcinogenic risk is found with the consumption of fresh chicken meat products on the food markets, while approximately 70% of the adult population in Guangzhou and 30% of those in Lianzhou have bladder and lung cancer risk above the serious or priority level (10⁻⁴), which arises from the inorganic arsenic contained in the chicken tissues. These findings indicate that the occurrence of inorganic arsenic at elevated levels in chicken tissues on the food markets in Guangdong province poses a significant public health risk, thus the use of phenylarsenic feed additives in China's poultry farming should be significantly reduced and eventually phased out.